In pharmacogenomics, the concept of 'phenoconversion' differs from genotyping in predicting drug metabolism. Phenoconversion refers to:

• A A poor metabolizer genotype converting to normal metabolizer status after induction of alternative CYP enzymes
• B Genetic testing changing the predicted metabolizer status from one phenotype to another upon re-testing
• C A normally extensive metabolizer becoming functionally a poor metabolizer due to co-administered CYP inhibitor drugs, disease states, or other factors ✓
• D Post-translational modification of CYP enzymes converting them from low-activity to high-activity forms

Explanation

Phenoconversion describes the discordance between an individual's genotypically predicted CYP metabolizer status and their actual (phenotypic) metabolizing capacity at a given time. The most clinically relevant form is an extensive metabolizer (normal CYP2D6 or CYP2C19 genotype) who becomes functionally a poor metabolizer due to concurrent strong CYP inhibition by drugs such as fluoxetine or paroxetine (for CYP2D6) or omeprazole (for CYP2C19), or due to liver disease reducing CYP expression. This means genotyping alone overestimates actual metabolizing capacity. Phenotyping (using probe drugs like dextromethorphan for CYP2D6) captures the phenoconverted state. Induction effects shifting poor to normal metabolizer is the opposite phenomenon.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.